Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Unanesthetized rats, made physically dependent over 5 days by chronic intra-arterial infusion of increasing concentrations of morphine (35-100 mg/kg/day) underwent withdrawal by naloxone (6 micrograms) injection into either the lateral ventricle (i.c.v.), fourth ventricle (V4), intrathecal subarachnoid space (i.t.), or intra-arterially (i.a.) and were evaluated for cardiovascular and behavioral signs of precipitated abstinence. Naloxone i.c.v. produced a significantly greater increase in the magnitude and duration of withdrawal hypertension than did V4 injection. Naloxone i.t. produced a distinctively different, persistent, pressor response as compared to i.c.v., V4 or i.a. routes of administration, although no quantitative differences in behavioral signs of withdrawal were observed. Morphine-dependent, spinal transected (C1) animals generated an augmented pressor response to i.c.v. or i.t. naloxone. This pressor response was accompanied by a significant reduction in core temperature (0.50-0.79 degrees C). Both the naloxone-induced pressor and hypothermic responses were abolished by ganglionic (hexamethonium, 100 mg/kg, i.a.) or peripheral alpha-adrenergic (phentolamine 4 mg/kg, i.a.) blockade. The hypertensive and hypothermic effects of naloxone also were prevented in transected dependent rats by prior spinal pithing. We conclude that in morphine-dependent rats: supraspinal sites rostral to the V4 mediate a more intense naloxone-induced pressor response than caudal regions; cardiovascular and behavioral signs of withdrawal can be precipitated via the spinal cord of intact animals; and the production of withdrawal hypertension and hypothermia in spinal transected morphine-dependent rats indicates that these abstinence signs can be mediated through neuronal pathways within the spinal cord.
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PMID:Supraspinal and spinal mediation of naloxone-induced morphine withdrawal in rats. 403 93

Proglumide has been reported to antagonize sulfated cholecystokinin octapeptide (CCK-8) in peripheral tissue and in neurophysiological single unit preparations. The present studies attempt to extend this reported antagonism to several actions of CCK-8 in mice in vivo. For comparison with proglumide, the antagonist activity of naloxone against CCK-8 has also been evaluated. Proglumide (150 mg/kg) antagonizes hot plate latency elevations produced by a moderate (0.17 mg/kg s.c.) dose of CCK-8, but not that by a higher (1.0 mg/kg) dose. The effects of intracerebroventricularly (i.c.v.) administered CCK-8 (0.3 micrograms) are also blocked by proglumide i.p. or i.c.v. Naloxone (0.5 mg/kg s.c.) significantly antagonizes the elevated hot plate latencies induced by CCK-8 i.c.v. (3.0 micrograms) and s.c. (3.0 mg/kg). Proglumide antagonizes the motor activity suppressant effects of CCK-8, but only at a high proglumide dose (150 mg/kg i.p.) and low CCK-8 doses. Naloxone (3.0 mg/kg) is not effective against CCK-8 in motor activity. The hypothermia induced by CCK-8 cannot be antagonized either by proglumide at doses up to 150 mg/kg i.p. or by naloxone at doses up to 3.0 mg/kg s.c. In vivo, proglumide may be considered as a weak antagonist of CCK-8 and the possibility exists that various actions of CCK-8 may be differentiated by their relative responsiveness to proglumide-induced antagonism.
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PMID:Differential antagonism by proglumide of various CCK-mediated effects in mice. 408 Jul 8

The effects of temperature on naloxone treatment in canine hemorrhagic shock were examined in 24 dogs hemorrhaged to a mean arterial blood pressure of 35 mm Hg (ambient temperature, 21 degrees C). After two hours of hypotension, the blood reservoir was clamped with no return of shed blood. Dogs were divided into three groups: Control (n = 8) received normal saline (0.5 cc/kg/hr); naloxone-cold (n = 8) and -warm (n = 8) received naloxone (2 mg/kg bolus and 2 mg/kg/hr constant infusion). Body temperature was maintained in four dogs with a warming blanket, and four dogs received no external warming. Rectal temperature fell to 34.2 +/- 0.9 degrees C in naloxone-cold animals; naloxone-warm animals were maintained at 38.6 +/- 0.1 degrees C by external warming. Control dogs rapidly deteriorated after reservoir clamping (survival, 18.6 +/- 5 min). Naloxone infusion significantly increased survival regardless of body temperature (cold, 125 +/- 21 min; warm, 199 +/- 13 min). Naloxone transiently increased mean arterial pressure and dP/dt in the colder dogs, while coronary perfusion, myocardial oxygen metabolism, and plasma beta-endorphin levels were unchanged. In the warmer dogs, naloxone significantly improved hemodynamic function and myocardial perfusion as indicated by the increased mean arterial pressure, cardiac output, stroke volume, dP/dt, and coronary blood flow. Furthermore, naloxone reduced plasma beta-endorphin levels and corrected the metabolic derangements of shock in this group. Our data indicate hypothermia significantly diminished the beneficial effects of naloxone treatment in canine hemorrhagic shock.
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PMID:Effect of temperature on naloxone treatment in canine hemorrhagic shock. 609 39

Circulatory shock and pain were associated as frequent consequences of surgery and trauma prior to the development of anesthetics. The recent discovery of the endogenous opioid systems affords the opportunity to link the occurrence of pain and circulatory shock at a functional level. The involvement of opioid systems in endogenously and exogenously induced analgesia is well established. In this review, evidence is presented indicating that endogenously activated opioid systems contribute to the pathophysiology of circulatory shock following such diverse causes as endotoxemia, hemorrhage, and spinal cord trauma. The opiate antagonist naloxone (Narcan), acting to oppose endogenous opiates, rapidly reverses the hemodynamic, metabolic, and biochemical sequelae of shock in experimental animal models. Additionally, naloxone has been shown to prevent paralysis following acute cervical spinal cord injury. As with all drugs, several physiologic and pathophysiologic circumstances limit the usefulness of naloxone in reversing shock and improving tissue perfusion. They include acidosis, hypothermia, interactions with administered steroids, and the potential for antagonizing opioid-induced analgesia, which may exacerbate pain in the traumatized patient. Two approaches have yielded potential ways to circumvent these limitations: first, the development of specific opioid-receptor antagonists, which reverse shock without affecting opioid analgesia, and second, the pharmacologic use of thyrotropin releasing hormone (TRH), which acts through its own effector system, independent of endogenous opioid receptors, to produce autonomic effects that reverse shock in experimental animals without affecting analgesia.
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PMID:Opiate antagonists in shock and trauma. 609 76

The influence of opiate receptor antagonists: naloxone, naltrexone and diprenorphine, and of an agonist: morphine on ethanol-induced sleep, hypothermia and motor coordination impairment was investigated. Naloxone and naltrexone evidently antagonized the sleep and hypothermia, and improved the motor coordination impaired by ethanol. Naltrexone was the most, and diprenorphine the least potent ethanol antagonist. Morphine potentiated only ethanol-induced sleep, and this effect was opiate dependent (reversible by naloxone). The present results may partially support the hypothesis about participation of opioid system in ethanol action. However, ethanol effects were affected only by high doses of opiate antagonists, exceeding by far the doses antagonizing the morphine effects. Therefore the participation of additional, unspecific mechanisms, in addition to an opiate-mediated one, cannot be excluded.
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PMID:Ethanol-opioid interaction in mice. 609 96

In this study we have examined the interactions of bombesin (1 microgram ICV), neurotensin (1 microgram ICV), TRH (10 micrograms ICV), somatostatin (10 micrograms ICV), PGE2 (10 micrograms ICV) and naloxone (10 mg/kg SC) on thermoregulation in the rat at room temperature (20 +/- 1 degree C). Given alone, bombesin, neurotensin, somatostatin and naloxone all produced hypothermia (bombesin greater than neurotensin greater than somatostatin congruent to naloxone). PGE2 was hyperthermic, and TRH had no effect. Bombesin and PGE2 neutralized one another's effects. Neurotensin had no effect on PGE2-induced hyperthermia. Naloxone enhanced the hypothermic effect of bombesin and somatostatin enhanced the rate of onset of hypothermia after bombesin. TRH had no effect on bombesin-induced hypothermia. TRH, somatostatin and naloxone had no effect on neurotensin-induced hypothermia. TRH antagonized the hypothermia due to naloxone and somatostatin.
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PMID:Neuropeptides and thermoregulation: the interactions of bombesin, neurotensin, TRH, somatostatin, naloxone and prostaglandins. 612 11

Di-isopropyl phosphofluoridate (DFP, 0.1--1.5 mg/kg, s.c.) produced antinociception in rats as measured by the hot plate test. Naloxone reduced DFP-induced antinociception but did not affect the attenuated locomotor activity or hypothermia produced by DFP. Animals rendered tolerant to the antinociceptive action of morphine failed to exhibit cross tolerance to the antinociceptive action of DFP. Morphine- and DFP-induced antinociceptive states were antagonized by MR 2266 and GPA 1843, the (-)-isomers of 5,9 alpha-Diethyl-2-(3-furylmethyl)-2'-hydroxy-6, 7-benzomorphan and -2-allyl-2'-hydroxy-9 beta-methyl-5-phenyl-6, 7-benzomorphan hydrochloride, respectively; the corresponding (+)-isomers, MR 2267 and GPA 1847, did not antagonize the antinociceptive state produced by DFP or morphine. These results suggest that DFP-induced antinociception may be mediated via the release of endogenous opioids; however, this could occur at sites different from those concerned with morphine tolerance.
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PMID:Di-isopropyl phosphofluoridate-induced antinociception: possible role of endogenous opioids. 624 66

Intracerebroventricular administration of 20, 40 and 60 nmol of dynorphin (1-13) produced analgesia, as assessed by flinch/jump response to footshock, and hypothermia in the rat. Rats developed tolerance to both the analgesic and thermic effects of the 20 nmol dose of dynorphin. Dynorphin and beta-endorphin showed cross-tolerance with respect to their analgesic but not their thermic effects. Dynorphin and morphine also produced cross-tolerant analgesic effects. Naloxone (10 mg/kg, IP) completely blocked the barrel rolling produced by 20 nmol dynorphin but did not alter its analgesic or thermic effects.
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PMID:Dynorphin (1-13): analgesia, hypothermia, cross-tolerance with morphine and beta-endorphin. 628 45

Phencyclidine elicits hyperthermia at low doses and hypothermia at high doses in rats. Naloxone antagonizes both effects. Phencyclidine's effects on thermo-regulation are probably mediated by an interaction with a mu opiate receptor.
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PMID:Naloxone antagonism of the thermoregulatory effects of phencyclidine. 628 81

Opioid peptides may act as neuromodulators in the central nervous system to conserve energy stores and water in mammals. To examine this hypothesis in man, the effect of opiate receptor blockade with naloxone on the hunger, thirst, and hypothermic response to 2-deoxy-D-glucose-induced glucoprivic stress was assessed. Opiate receptor blockade decreased stress-induced food intake but did not reduce marked increases in hunger produced by glucoprivation. Naloxone infusions did not change the hypercortisolemic, polydipsic, hypothermic, and thermogenic response to 2-deoxy-D-glucose. While these results do not suggest a major role for a beta-endorphin modulation of stress-induced hunger, hypothermia and water conservation, the reduction of food intake could be due to augmented satiety, perhaps associated with retardation of gastric emptying during opiate receptor blockade.
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PMID:Opiate receptor blockade in man reduces 2-deoxy-D-glucose-induced food intake but not hunger, thirst, and hypothermia. 629 33


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